Impact of Visceral Obesity on the Risk of Incident Metabolic Syndrome in Metabolically Healthy Normal Weight and Overweight Groups: A Longitudinal Cohort Study in Korea.
Body Mass Index
Follow-Up Studies
Metabolic Syndrome
Metabolically Healthy Obesity
Visceral Obesity
Journal
Korean journal of family medicine
ISSN: 2005-6443
Titre abrégé: Korean J Fam Med
Pays: Korea (South)
ID NLM: 101502902
Informations de publication
Date de publication:
Jul 2020
Jul 2020
Historique:
received:
30
07
2018
accepted:
23
10
2018
pubmed:
30
4
2020
medline:
30
4
2020
entrez:
30
4
2020
Statut:
ppublish
Résumé
Although both obesity, measured by body mass index, and visceral obesity are known to be major risk factors of metabolic syndrome and its components, there have been debates on the relative contribution of general obesity and visceral obesity to the development of metabolic syndrome. We performed a large longitudinal cohort study of 3,093 subjects (age range, 18-65 years) who were metabolically healthy and had a normal weight who received health screenings over a 3-year follow-up period. Cox proportional hazards models were used to estimate the adjusted hazard ratios (HRs) and 95% confidence intervals (CI) for incident metabolic syndrome and its components per sex-specific 1-standard deviation (SD) increase in visceral adipose tissue (VAT) and body mass index. Both obesity and visceral obesity increased the risk of incident metabolic syndrome, but when HR was compared per sex-specific 1-SD, visceral obesity appeared to confer more risk than simple obesity. The HR for 1-SD of body mass index was 1.19 (95% CI, 1.07-1.32; P=0.001) in men and 1.29 (95% CI, 1.10-1.52; P=0.002) in women, while the HR for 1-SD of VAT was 1.29 (95% CI, 1.15-1.44; P<0.001) in men and 1.50 (95% CI, 1.28-1.75; P<0.001) in women. Visceral obesity and obesity were longitudinally associated with an increased risk of incident metabolic syndrome among metabolically healthy adults, and visceral fat accumulation appears to be better predictor of metabolic syndrome.
Sections du résumé
BACKGROUND
BACKGROUND
Although both obesity, measured by body mass index, and visceral obesity are known to be major risk factors of metabolic syndrome and its components, there have been debates on the relative contribution of general obesity and visceral obesity to the development of metabolic syndrome.
METHODS
METHODS
We performed a large longitudinal cohort study of 3,093 subjects (age range, 18-65 years) who were metabolically healthy and had a normal weight who received health screenings over a 3-year follow-up period. Cox proportional hazards models were used to estimate the adjusted hazard ratios (HRs) and 95% confidence intervals (CI) for incident metabolic syndrome and its components per sex-specific 1-standard deviation (SD) increase in visceral adipose tissue (VAT) and body mass index.
RESULTS
RESULTS
Both obesity and visceral obesity increased the risk of incident metabolic syndrome, but when HR was compared per sex-specific 1-SD, visceral obesity appeared to confer more risk than simple obesity. The HR for 1-SD of body mass index was 1.19 (95% CI, 1.07-1.32; P=0.001) in men and 1.29 (95% CI, 1.10-1.52; P=0.002) in women, while the HR for 1-SD of VAT was 1.29 (95% CI, 1.15-1.44; P<0.001) in men and 1.50 (95% CI, 1.28-1.75; P<0.001) in women.
CONCLUSION
CONCLUSIONS
Visceral obesity and obesity were longitudinally associated with an increased risk of incident metabolic syndrome among metabolically healthy adults, and visceral fat accumulation appears to be better predictor of metabolic syndrome.
Identifiants
pubmed: 32344994
pii: kjfm.18.0122
doi: 10.4082/kjfm.18.0122
pmc: PMC7385301
doi:
Types de publication
Journal Article
Langues
eng
Pagination
229-236Références
Diabet Med. 2008 Jan;25(1):106-10
pubmed: 18028439
J Am Geriatr Soc. 2010 Sep;58(9):1658-63
pubmed: 20863325
Sci Rep. 2017 Sep 8;7(1):10955
pubmed: 28887474
Obesity (Silver Spring). 2006 Feb;14 Suppl 1:16S-19S
pubmed: 16642958
Proc Jpn Acad Ser B Phys Biol Sci. 2012;88(8):454-61
pubmed: 23060233
Lancet Diabetes Endocrinol. 2013 Oct;1(2):152-62
pubmed: 24622321
Endocrine. 2014 Nov;47(2):500-5
pubmed: 24504765
J Clin Endocrinol Metab. 2011 May;96(5):1462-8
pubmed: 21325457
Rev Endocr Metab Disord. 2013 Sep;14(3):219-27
pubmed: 23928851
Diabetes Metab Syndr. 2017 Dec;11 Suppl 2:S957-S961
pubmed: 28711515
Circulation. 2007 Jul 3;116(1):39-48
pubmed: 17576866
J Korean Med Sci. 2011 Jul;26(7):906-13
pubmed: 21738344
Circulation. 2005 Oct 25;112(17):2735-52
pubmed: 16157765
Diabetes Care. 2011 Feb;34(2):504-6
pubmed: 21228245
J Clin Invest. 2004 Dec;114(12):1752-61
pubmed: 15599400
Am J Cardiol. 2009 Jul 15;104(2):240-6
pubmed: 19576354
Lancet. 2004 Jan 10;363(9403):157-63
pubmed: 14726171
Indian J Med Res. 2010 May;131:629-35
pubmed: 20516533
JAMA. 2003 Jan 1;289(1):76-9
pubmed: 12503980
Diabetes Care. 2001 Apr;24(4):683-9
pubmed: 11315831
Metabolism. 2010 Mar;59(3):333-7
pubmed: 19796779
Int J Obes (Lond). 2015 Sep;39(9):1365-70
pubmed: 25920773
Circulation. 2004 Jan 27;109(3):433-8
pubmed: 14744958
Gut. 2008 Oct;57(10):1360-5
pubmed: 18441006
AJR Am J Roentgenol. 2012 May;198(5):1100-7
pubmed: 22528899
JACC Cardiovasc Imaging. 2014 Dec;7(12):1221-35
pubmed: 25440591
Liver Int. 2017 Jun;37(6):919-926
pubmed: 27917585
PLoS One. 2017 Jun 23;12(6):e0179635
pubmed: 28644850